In humans, disorders of the optic nerve, such as ischemic optic neuropathy and some primary optic nerve tumors, can have combined histopathologic effects on the nerve and the macula, leading to cell death and visual decline. In mammals, injury to axons within the central nervous system leads almost inevitably to the death of the axotomized neurons. Those few which survive are unable to regenerate successfully because of the inhibitory properties of CNS glia. The axons of amphibia do not have to contend with this glial inhibition, they successfully regenerate after injury despite a considerable ganglion cell loss in the retina. This makes the frog optic nerve, which is a particularly considerable ganglion cell loss in the retina. This makes the frog optic nerve, which is a particularly accessible CNS tract, a good model system in which to study the effects that damaging the optic nerve have on ganglion cell death in the retina. The long term goal of this research is to elucidate the factors that determine which of the retinal ganglion cells undergo cell death after axotomy, and to determine if it is possible to rescue some of those ganglion cells from dying. This project aims firstly to quantify the numbers and types of ganglion cells which survive after cutting the optic nerve, both when regeneration proceeds normally or is curtailed. The second aims is to study the ways in which the surviving retinal ganglion cells compensate for the loss of their neighbors by remodeling their dendrites. The third aim will quantify the effects on retinal ganglion cell survival of manipulating the optic nerve stump environment by changing the number and type of glial cells that surround the axons. The fourth aim is to determine if growth factors can increase the number of cells surviving axotony. In the long term this model may prove useful for increasing our knowledge of the basic mechanisms that can rescue nerve cells from death after damage.